Cardiac arrhythmias can result in a range of uncomfortable and life-threatening conditions for patients. A normally-functioning heart relies on coordinated delays in the propagation of electrical impulses through cardiac tissue. Blocked or abnormal electrical conduction through cardiac tissue can cause dysynchronous contraction, and can reduce hemodynamic efficiency and cardiac output. Deteriorated cardiac tissue can encourage arrhythmic behavior and can result in compromised blood supply to the heart, and to the rest of the body, as well as the possibility of thromboembolism, stroke, or even death.
Tachyarrhythmias can be thought of as abnormal heart rhythms characterized by a too-rapid heart rate. Examples of ventricular tachyarrhythmias include ventricular tachycardia (VT), and ventricular fibrillation (VF). Ventricular arrhythmias can be caused by waves of depolarization propagating through cardiac tissues of differing electrical characteristics (e.g., differences in propagation delay, refractory time). A self-sustaining reentrant depolarization wave with one or more foci can usurp control of heart rate from the sino-atrial (SA) node. Such reentrancy can allow the ventricular contraction rate to run away, resulting in abnormally fast, uncoordinated, and inefficient ventricular contractions, such as in the case of VT. Anti-tachyarrhythmia pacing (ATP) therapy, ventricular shock therapy, or a combination can be provided by a cardiac rhythm management device to restore a normal sinus rhythm before the VT degenerates into life-threatening VF.
VF can be occurring if no identifiable QRS complexes or coordinated contractions of the ventricles are present. Shock therapy from, for example, an automated implantable cardioverter defibrillator (AICD), cardiac resynchronization therapy device with defibrillation backup (CRT-D), or an external defibrillator can be provided to convert the VF to a normal sinus rhythm.